The Journal of Nutrition

Nutrition and Disease

Cashew Nut Consumption Increases HDL

Cholesterol and Reduces Systolic Blood
Pressure in Asian Indians with Type 2
Diabetes: A 12-Week Randomized Controlled
Trial
Viswanathan Mohan,1 Rajagopal Gayathri,2 Lindsay M Jaacks,3 Nagarajan Lakshmipriya,2

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Ranjit Mohan Anjana,1 Donna Spiegelman,3,4 Raman Ganesh Jeevan,2 Kandappa K Balasubramaniam,2
Shanmugam Shobana,2 Mathialagan Jayanthan,2 Viswanathan Gopinath,2 Selvakumar Divya,2
Vasudevan Kavitha,2 Parthasarathy Vijayalakshmi,2 Mookambika Ramya Bai R,2 Ranjit Unnikrishnan,1
Vasudevan Sudha,2 Kamala Krishnaswamy,2 Jordi Salas-Salvadó,6 and Walter C Willett4,5

Departments of 1 Diabetology and 2 Foods, Nutrition & Dietetics Research, Madras Diabetes Research Foundation, Chennai, Tamil Nadu,
India; Departments of 3 Global Health and Population, 4 Nutrition, and 5 Epidemiology, Harvard T.H. Chan School of Public Health, Boston,
MA and 6 Human Nutrition Unit, Hospital Universitari Sant Joan de Reus, Biochemistry and Biotechnology Department, IISPV, Universitat
Rovira i Virgili, Reus, Spain, and CIBERobn Physiopathology of Obesity and Nutrition, Instituto de Salud Carlos III, Madrid, Spain

Abstract
Background: There is increasing evidence that nut consumption decreases the risk of cardiovascular disease. However,
there are few data on the health effects of cashew nuts among adults with type 2 diabetes (T2DM).
Objective: The study aimed to investigate the effects of cashew nut supplementation on glycemia, body weight, blood
pressure, and lipid profile in Asian Indians with T2DM.
Methods: In a parallel-arm, randomized controlled trial, 300 adults with T2DM [mean ± SD age: 51 ± 9.3 y; body
mass index (BMI; in kg/m2 ): 26.0 ± 3.4; 55% male] were randomly assigned to receive advice to follow a standard
diabetic diet (control) or similar advice plus 30 g cashew nuts/d (intervention) for 12 wk. The macronutrient composition
of the prescribed diabetic diet was 60–65% energy from carbohydrates, 15–25% from fat, and the rest from protein.
Differences between groups in changes in anthropometric and biochemical variables were analyzed using linear models
with robust variance estimation under an assumed independence working correlation.
Results: Participants in the intervention group had a greater decrease in systolic blood pressure from baseline to
12 wk than did controls (–4.9 ± 13.7 compared with –1.7 ± 11.6 mm Hg; P = 0.04) and a greater increase in plasma HDL
cholesterol compared with controls (+1.7 ± 5.6 compared with +0.1 ± 4.6 mg/dL; P = 0.01). There were no differences
between the groups with respect to changes in body weight, BMI, blood lipid, and glycemic variables. Plasma oleic acid
concentrations and self-reported dietary intake of nuts, oleic acid, and monounsaturated fatty acids suggested excellent
compliance with the nut consumption.
Conclusion: Cashew nut supplementation in Asian Indians with T2DM reduced systolic blood pressure and
increased HDL cholesterol concentrations with no deleterious effects on body weight, glycemia, or other lipid variables.
This study was registered at the clinical trial registry of India as CTRI/2017/07/009022. J Nutr 2018;148:63–69.

Keywords: cashew nut, type 2 diabetes, high-density lipoprotein cholesterol, body weight

Introduction and 98% of females have been shown to have dyslipidemia (4).
Although the link between low HDL cholesterol and CVD is es-
Populations of Asian Indian ethnicity are characterized by a
tablished (5), current evidence suggests that raising HDL choles-
high lifetime risk of cardiovascular disease (CVD) and type 2
terol using pharmacologic approaches is challenging and may
diabetes (T2DM) (1). Asian Indians are prone to a unique pat-
not directly translate into reduced CVD risk (6).
tern of dyslipidemia characterized by low HDL cholesterol and
Current Indian diets are high in carbohydrates (predomi-
high TGs and LDL cholesterol (2). Nearly 80% of Asian Indian
nantly derived from refined grains such as polished rice and
adults have dyslipidemia, largely driven by low HDL cholesterol
refined wheat), which account for 64% of total energy intake
concentrations (3). Among those with T2DM, 86% of males
(7). Indian diets are low in MUFAs, which provide just 7–8%

© 2018 American Society for Nutrition. All rights reserved.

Manuscript received March 31, 2017. Initial review completed May 12, 2017. Revision accepted October 17, 2017. 63
First published online January 25, 2018; doi: https://doi.org/10.1093/jn/nxx001.
of total energy (8) compared to the recommended intake of 15–
20% (9), as well as omega-3 PUFAs, which provide just 0.24%
of total energy compared to the recommended intake of 0.5–
2% (9, 10). Consumption of nuts, a rich source of MUFAs, has
historically been low in India (8 g/d in 1975–79 and 17 g/d in
1996–97) (11). There is growing evidence that replacement of
refined grains with healthy fats such as MUFAs may have ben-
eficial effects on HDL cholesterol (12) and that daily intake of
∼60 g of nuts may also improve diabetes control through reduc-
tion in fasting blood glucose and glycosylated hemoglobin A1c
(13). Moreover, a recent meta-analysis of clinical trials indicates
that nuts, despite their higher fat and energy content, have no
significant effects on body weight when substituted in a healthy
diet (14). This is important as weight control is crucial for pre-
vention of diabetes and diabetes-related complications (15).
Previous studies have focused on the beneficial health effects
of nuts, including pistachios, walnuts, and almonds, on insulin
resistance and other CVD risk factors (16–19). Only one study
has evaluated the effects of cashew nuts on CVD risk factors.
Subjects with metabolic syndrome were randomly assigned to
receive 66–115 g cashew nuts/d or a control diet for 8 wk; no
significant effects were observed for the lipid variables evaluated
(20). This could be due to the fact that baseline lipid concentra-
tions (LDL cholesterol) were already low, the small sample size
(n = 64), the short duration of the intervention, ethnicity, or
other factors.
To date, though widely used in Indian cuisines, cashew nuts
have not been evaluated for their potential effects on CVD risk
factors among Asian Indians, particularly those with T2DM.
The aim of this parallel-arm, randomized controlled trial was to
test the effect of cashew nut supplementation on glycemia (pri-
mary outcome) and body weight, blood pressure and lipid pro-
files (secondary outcomes) in Asian Indian adults with T2DM.
The primary hypothesis was that diets supplemented with
30 g unsalted cashew nuts/d would result in improvements in
glycemic status among Asian Indians with T2DM.
Methods
Study participants. Participants in this parallel-arm, randomized
controlled trial were identified from the medical records of a tertiary
care center for diabetes in Chennai, India, based on prespecified in-
clusion and exclusion criteria. Inclusion criteria were: age 30–65 y,
physician-diagnosed T2DM, duration of T2DM <10 y, and currently re-
ceiving oral hypoglycemic drugs. Exclusion criteria were: cashew nut al-
lergy, currently receiving insulin therapy, glycated hemoglobin (HbA1c)
>10%, LDL cholesterol >190 mg/dL, total cholesterol >240 mg/dL,
TGs >300 mg/dL, and any known diabetes complications.
Eligible participants identified via this medical record review
(n = 500) were then contacted and briefed by research dieticians about
The main sponsor for the study was the Cashew Export Promotion Council of
India, Kollam supported by the Department of Commerce, Ministry of Com-
merce & Industry, Government of India. We acknowledge the co-sponsors of the
study for their financial support: Samsons Trading Company Pvt. Ltd., Mumbai,
Maharashtra, India; Kerala Nut Food Company, Kollam, Kerala, India; Alphonsa
Cashew Industries, Kollam, Kerala, India; Cashew Manufacturers Association,
Mangalore, Karnataka, India; Western India Cashew Company Pvt. Ltd., Kollam,
Kerala, India; and Intersnack Procurement BV, The Netherlands.
Author disclosures: VM, RG, LMJ, NL, RMA, DS, RGJ, KKB, SS, MJ, VG, SD,
VK, PV, MRB, RU, VS, KK, JS-S, and WCW, no conflicts of interest.
Supplemental Table 1 is available from the “Supplementary Data” link in the
online posting of the article and from the same link in the online table of contents
at https://academic.oup.com/jn.
Address correspondence to VM (e-mail: drmohans@diabetes.ind.in).
Abbreviations used: CVD, cardiovascular disease; HbA1c, glycated hemoglobin;
SBP, systolic blood pressure; T2DM, type 2 diabetes.
64 Mohan et al.
the study and its objectives (Figure 1). Individuals expressing an in-
terest in participating were given 30 g cashew nuts/d for 1 wk (run-
in period) free of cost in order to ensure compliance. Individuals who
completed the run-in period and expressed their willingness to com-
ply and take part in the study were randomized to either intervention
(n = 150) or control (n = 150) groups and completed the baseline visit
2 wk after the run-in period.
Written informed consent was obtained from all participants. The
study received approval from the Institutional Ethics Committee of the
Madras Diabetes Research Foundation and was conducted in accor-
dance with guidelines in the Declaration of Helsinki. The study was
registered at the clinical trial registry of India as CTRI/2017/07/009022.
Dietary intervention. Participants assigned to the intervention
group were provided with 30 g unsalted, raw, broken cashew
nuts/d free of charge on a weekly basis for 12 wk. This quan-
tity was based on previous studies that have used similar amounts:
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the PREvención con DIeta MEDiterránea (PREDIMED) study used
30 g mixed nuts/d (18) and Tapsell et al. (21) in their ran-
domized trial used 30 g walnuts/d. The cashew nuts constituted
∼11–13% of prescribed diabetic diet calories (∼182 kcal/30 g
cashew nut) (22). Participants were advised to consume the cashew nuts
either as a mid-morning or evening snack, and to maintain their pre-
scribed standard diabetic diet, exercise, and medication as usual. The
cashew nut group (intervention) participants were further instructed
not to use the cashew nuts as a cooking ingredient or to roast or fry
them, and not to consume any nuts other than the allotted quantity of
cashew nuts. They were further taught to substitute the calories from
30 g cashew nuts with equivalent calories from carbohydrates in their
meals. Participants assigned to the control group were advised to fol-
low their prescribed standard diabetic diet, exercise, and medications as
usual. Control participants were also advised not to consume any other
type of nuts.
For both groups, all dietary advice was individualized and provided
by dietitians, as is standard practice for the tertiary care center for di-
abetes in Chennai, India, where this study was conducted. The Asian
Indian diabetic diet (1400–1600 kcal/d) upon which advice was based
is typically composed of 60–65% energy from carbohydrates, 15–25%
from fat, and the remaining calories from protein (23). A review with
dietitians took place every 4 wk throughout the duration of the study.
In-person monthly interviews were carried out by trained dietitians to
collect 24-h dietary recalls (1 weekday and 1 weekend). A total of 6
dietary recalls were performed over 12 wk, including a single 24-h re-
call at baseline for the participants in both groups. The average of the
5 recalls collected during the intervention (second recall at the end of
the fourth week, third and fourth recalls between 5 and 8 wk, fifth and
sixth recalls between 9 and 12 wk) was compared with the single recall
collected at baseline in order to improve the precision and accuracy of
the estimates of dietary intake during the intervention period.
Participant compliance. Participant compliance was assessed us-
ing 1) self-reported dietary intake by 24-h dietary recall administered
by trained dietitians in a face-to-face interview (the average of 5 recalls
collected during the 12-wk intervention was compared to baseline); and
2) a plasma biomarker of the predominant MUFA, oleic acid (the con-
centrations at 12 wk compared to baseline) (24). Participants assigned
to the intervention group were also asked 3) to return the empty sachets
of cashew nuts every week. In an attempt to avoid any sharing of the
30 g cashew nut supplement with family members, an additional 200-g
cashew nut sachet was supplied to each participant in the intervention
group during weekly visits. We did not have a prespecified compliance
cutoff nor did we remove noncompliant participants from the analysis;
this information was primarily collected in order to facilitate the inter-
pretation and translation of study results.
Nutrient intake (total calories and percentage of calories from
SFAs, MUFAs, PUFAs, trans fatty acids, oleic acid, total fat, carbohy-
drates, protein, and cholesterol) was estimated from the 24-h dietary
recalls using the nutrient database EpiNu (25). Plasma oleic acid was
determined by the method described by Glaser et al. (26) as refer-
ence method and that of Folch et al. (27) for oleic acid methyl ester

FIGURE 1 Study flow diagram for randomized controlled trial of a cashew nut supplement (30 g/d) among adults with type 2 diabetes con-
suming a standard prescribed diabetic diet (control). $ Nonresponsive to follow-up despite repeated attempts to reach participants in both groups
by telephone after baseline visit, and hence, considered dropouts.
preparation with minor modifications—the final volume of the sample
made up for GC analysis was 1 mL compared with 50 µL referred by the
method, and the centrifuge was used at 1350 × g in contrast to 900 × g
for a comparable time. Oleic acid methyl ester was quantified with
flame ionization detection on a Shimadzu GC-2010 plus gas chromato-
graph using an Agilent DB-Wax column (30 m, 0.250 mm diameter, film
0.25 µm). Data were acquired using Lab Solutions software version
5.52. The qualitative and quantitative processing of the integrated peaks
was achieved with a mixture of standard fatty acids (Lot No. 24305 and
Catalogue No. 35077, Restek). The intra- and inter-day CV were 3.3%
and 3%, respectively. Plasma oleic acid methyl ester was quantified using
standard oleic acid (Batch No. BCBQ2570V and Product No. 75090,
Sigma Aldrich) for comparison.
Outcome assessment. Glycemic and lipid profiles were assessed
in a laboratory certified by the National Accreditation Board for Test-
ing and Calibration Laboratories and the College of American Pathol-
ogists on a Hitachi 912 Autoanalyzer. Fasting (≥8 h) venous whole
blood samples were collected at baseline and at the end of the study
(12 wk) into tubes containing EDTA as an anticoagulant. Plasma
glucose was estimated using the glucose oxidase-peroxidase method
(Roche Diagnostics). HbA1c was estimated by HPLC (Variant; Bio-
Rad) and serum insulin by electrochemiluminescence assay (Roche
Diagnostics). Insulin resistance was calculated using the homoeosta-
sis model assessment (28). A Beckman Coulter AU 2700/480 Auto-
analyzer was used to measure serum cholesterol (cholesterol esterase
oxidase-peroxidase-amidopyrine method), serum TG (glycerol phos-
phate oxidase-peroxidase-amidopyrine method), and HDL cholesterol
by direct method with polyethylene glycol-pretreated enzymes. LDL and
VLDL cholesterol were calculated using the Friedewald formula (29).
The coefficients of variation for the biochemical assays ranged from
3.1% to 7.6% (30).
Body weight (kilograms) (Omron HBF 212), height (centimeters),
and waist circumference (centimeters) were measured at baseline and
at the end of the study (12 wk) according to standard protocols. BMI
was calculated as weight divided by squared height (kg/m2 ). Blood
pressure was measured at baseline and end of study (12 wk) using an
electronic monitor (Omron HEM 7120). Participants were seated com-
fortably with back straight and feet flat on the floor. Blood pressure
was assessed twice on each occasion at 5-min intervals and the average
reading was taken (31).
Statistical analysis. Differences in baseline characteristics between
the intervention and control groups were tested using chi-square tests
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and independent sample 2-sided t tests. Between-group differences in the
change in dietary intake and the health measurements between baseline
and 12 wk were analyzed using linear models with robust variance es-
timation under an assumed independence working correlation. This is
equivalent to a 2-sample (independent group) t test with the exception
of the variance estimation in that we used robust variance estimation to
account for nonnormality of the data. Missing outcome data were not
imputed, and thus this was a partial intent-to-treat analysis. As a sensi-
tivity analysis, we compared mean change in HDL cholesterol between
intervention participants with low- compared with high-HDL choles-
terol at baseline (for women, HDL cholesterol <50 compared with
≥50 mg/dL; for men, HDL cholesterol <40 compared with ≥40 mg/dL)
using a t test, and also calculated the Pearson correlation coefficient be-
tween changes in plasma oleic acid concentration and changes in HDL
cholesterol, stratified by intervention compared with control group. A
2-tailed P value <0.05 was considered statistically significant. Statistical
analyses were performed using SAS software, version 9.4 (SAS Institute
Inc.).
Results
Of the 300 participants enrolled, 269 (89.7%) completed the
end-of-study visit at 12 wk (Figure 1). Results herein are re-
ported for the 269 participants who completed the study. The
study participants’ age was 50.8 ± 9.5 y (mean ± SD) and
53.9% (n = 145) were men. There was a higher percentage of
men in the intervention group compared to the control group
(P = 0.04; Table 1).
As a measure of compliance in the intervention group par-
ticipants, 83% returned the empty sachets for the entire study
period while 10% of the participants returned empty sachets
for 2–4 wk. Plasma oleic acid concentrations increased signifi-
cantly (P = 0.001) from baseline in the intervention group com-
pared to the control group (Table 2). Consistent with this, there
was a significantly greater increase in self-reported intake of
nuts, MUFAs, and oleic acid (as percentage of energy) in the
intervention group (Table 2) compared to the control group.
However, the correlation between changes in plasma oleic acid
concentrations and changes in HDL cholesterol (Supplemental
Table 1) were nonsignificant.
Effect of cashew nuts on glycemic and lipid profile 65
TABLE 1 Baseline characteristics of participants with type 2 Discussion
diabetes who completed the study, randomly assigned to either
a cashew nut supplement group (30 g/d) or a control group To our knowledge, this is the first randomized controlled trial to
(n = 269)1 assess the effect of cashew nut supplementation on blood pres-
sure, serum lipids, body weight, and glycemia in Asian Indian
Cashew nut adults with T2DM. The key findings of the study include a sig-
supplement Control nificant increase in HDL cholesterol concentrations and a sig-
group group P nificant decrease in SBP in the intervention group supplemented
Characteristics (n = 129) (n = 140) value2 with 30 g cashew nuts/d over 12 wk compared to the con-
Age, y 51.3 ± 8.8 50.4 ± 10.1 0.43 trol (standard of care) group. Moreover, despite a significantly
Male, % (n) 60.5 (78) 47.9 (67) 0.04 greater reported increase in caloric intake among the interven-
Duration of diabetes, y 6.0 ± 3.9 5.6 ± 4.5 0.51 tion participants, there was not a significant increase in body
Current smoker, % yes (n) 3.1 (4) 2.1 (3) 0.62 weight, BMI, or waist circumference.
Consume alcohol, % yes (n) 9.3 (12) 6.4 (9) 0.38 There is a misconception in India that eating nuts increases
Oral hypoglycemic agent(s), % yes (n) 74.4 (96) 70.7 (98) 0.42 body weight due to their high fat content and energy density
Medication for hypertension, % yes (n) 14.8 (19) 12.1 (17) 0.51 (32). This study showed that consumption of moderate amounts

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Medication for dyslipidemia, % yes (n) 15.5 (20) 9.3 (13) 0.12 of cashew nuts did not increase body weight, BMI, waist circum-
ference, serum cholesterol or LDL cholesterol. This supports
1
Values are means ± SDs or percentage (n).
2
P-value from chi-square test (binary variables) or independent sample 2-sided t test the findings from earlier studies on pistachios, walnuts and al-
(continuous variables) comparing cashew nut supplement group and control group monds (16–19, 33, 34). A meta-analysis of clinical trials of the
characteristics at baseline. effects of tree nuts, including almonds, walnuts, and pistachios,
on adiposity showed that nut-rich diets did not increase body
weight, BMI, waist circumference, or serum cholesterol com-
pared with different control diets. Hence, it was suggested to
Participants in the intervention group had a 1.9-fold greater
include nuts as part of healthy diets for prevention of obesity-
reduction in systolic blood pressure (SBP) compared to partic-
related chronic diseases including CVD (14). Furthermore, trials
ipants in the control group (Table 3). Participants in the in-
of nuts alone or nuts as part of the Mediterranean diet or as Di-
tervention group also had a 16-fold greater increase in HDL
etary Approaches to Stop Hypertension (DASH) trial patterns
cholesterol compared to participants in the control group. When
have shown neutral or weight-loss effects (17, 35–37). Petersen
participants were stratified by their baseline HDL cholesterol
et al. (20) investigated the effects of walnuts, unsalted cashew
status, we observed a mean (SD) change of +2.2 (5.7) mg/dL
nuts, and a “no nuts diet” on selected markers of the metabolic
among participants in the low–HDL cholesterol category
syndrome. They showed that following a walnut or cashew nut
(n = 98) in the intervention group compared to a mean (SD)
diet for 8 wk was not associated with weight gain. There are
change of 0.0 (4.9) mg/dL among participants in the interven-
several possible mechanisms that could explain the observation
tion group with high HDL cholesterol (n = 31) at baseline
that increased nut consumption had a neutral effect on body
(P = 0.04). When models were adjusted for differences between
weight. Nuts including cashews are high in readily oxidizable
groups in baseline sex, the results for SBP were slightly atten-
MUFAs and PUFAs, which may increase their thermogenic ef-
uated (P = 0.05), but all other results were consistent. There
fect (14). Studies have also suggested that incomplete mastica-
were no significant changes in other serum lipid variables, fast-
tion of nuts leads to loss of calories in the stool (38, 39). Mori
ing plasma glucose, fasting insulin, HbA1c, body weight, BMI,
et al. (40) showed that including nuts in breakfast could improve
or waist circumference between the 2 groups.

TABLE 2 Markers of dietary compliance (by self-reported average 24-h dietary recalls) of participants with type 2 diabetes who
completed the study, randomly assigned to either a cashew nut supplement group (30 g/d) or a control group (n = 269)1

Cashew nut supplement group Control group

Between-group
Baseline 12 wk Change Baseline 12 wk Change difference in within-group
(n = 129) (n = 129) (n = 129) (n = 140) (n = 140) (n = 140) changes (95% CI)2 P value2
Plasma oleic acid, µmol/L 303 ± 338 451 ± 529 90.8 ± 432 703 ± 569 526 ± 493 –190 ± 765 280 (107, 453) 0.001
Nuts and oil seed, g/d 13.0 ± 14.6 48.7 ± 33.9 35.7 ± 37.2 12.6 ± 15.7 11.3 ± 9.5 –1.1 ± 17.8 36.8 (29.8, 43.7) <0.0001
Cashew nut, g/d 1.1 ± 1.7 31.9 ± 3.5 30.7 ± 4.0 0.5 ± 0.8 0.9 ± 5.1 0.5 ± 5.5 30.2 (29.0, 31.4) <0.0001
MUFAs,3 %E 7.7 ± 2.3 9.3 ± 2.1 1.6 ± 2.9 8.0 ± 2.5 7.0 ± 1.3 –1.1 ± 2.6 2.7 (2.0, 3.3) <0.0001
PUFAs,3 %E 10.4 ± 3.1 9.5 ± 7.3 –0.7 ± 3.9 10.2 ± 3.4 10.6 ± 3.4 0.5 ± 4 –1.0 (–1.9, 0.04) 0.03
TFAs,3 %E 0.1 ± 0.1 0 ± 0.1 0 ± 0.1 0.1 ± 0.2 0 ± 0.1 0 ± 0.1 0 (–0.04, 0.03) 0.92
SFAs,3 %E 9.0 ± 3.2 7.9 ± 2.3 –0.7 ± 4.4 9.2 ± 3.5 7.6 ± 2.6 –1.3 ± 5 0.4 (–0.4, 1.3) 0.42
Cholesterol, mg/d 83.3 ± 125.4 45.2 ± 48.0 –38.7 ± 114.4 97.1 ± 161.5 49.9 ± 72.1 –47.8 ± 177.7 0.07 (–27.6, 45.7) 0.63
Oleic acid,3 %E 7.2 ± 2.2 8.6 ± 1.8 1.4 ± 2.8 7.5 ± 2.4 6.5 ± 1.3 –1.0 ± 2.5 2.3 (1.7, 3.0) <0.0001
Energy, kcal/d 1536 ± 467 1598 ± 415 68.4 ± 489 1532 ± 508 1451 ± 355 –77.9 ± 464 146.3 (30.8, 261.8) 0.01
Carbohydrate,3 %E 59.1 ± 6.4 57.9 ± 4.2 –1.2 ± 7.0 58.1 ± 8.5 61.4 ± 4.3 3.3 ± 8.8 –4.5 (–6.5, 2.6) <0.0001
Protein,3 %E 12.8 ± 2.7 11.8 ± 1.1 –1.0 ± 2.7 13.4 ± 3.1 11.7 ± 1.4 –1.7 ± 3.3 0.7 (–0.04, 1.4) 0.06
Fat,3 %E 28.7 ± 5.5 30.4 ± 4.0 1.7 ± 6.4 28.9 ± 6.8 27.0 ± 4.0 –1.9 ± 7.2 3.7 (2, 5.3) <0.0001
1
Values are means ± SDs. TFA, trans fatty acid; %E, percentage of energy.
2
From linear models with robust variance estimation under an assumed independence working correlation.
3
Values may not add up to 100% due to rounding.

66 Mohan et al.
TABLE 3 Anthropometric and biochemical characteristics of participants with type 2 diabetes who completed the study, randomly
assigned to either a cashew nut supplement group (30 g/d) or a control group (n = 269)1

Cashew nut supplement group Control group

Between-group
Baseline 12 wk Change Baseline 12 wk Change difference in within-group
(n = 129) (n = 129) (n = 129) (n = 140) (n = 140) (n = 140) changes (95% CI)2 P value2
Weight, kg 67.6 ± 9.1 67.9 ± 9.0 0.2 ± 1.1 67.3 ± 11.5 67.2 ± 11.5 –0.1 ± 1.7 0.32 (–0.02, 0.65) 0.07
BMI, kg/m2 25.6 ± 2.8 25.7 ± 2.7 0.1 ± 0.4 26.2 ± 3.9 26.2 ± 3.9 0.0 ± 0.6 0.12 (–0.01, 0.25) 0.07
WC, cm 91.0 ± 8 91.2 ± 7.9 0.1 ± 2.3 90.7 ± 9.3 90.9 ± 9.3 0.3 ± 2.6 –0.12 (–0.71, 0.46) 0.69
SBP, mm Hg 125.5 ± 15.1 121 ± 14.0 –4.9 ± 13.7 123.6 ± 15.9 122 ± 15.1 –1.7 ± 11.6 –3.15 (–6.17, –0.12) 0.04
DBP, mm Hg 82.3 ± 9.1 81.2 ± 8.8 –1.0 ± 7.9 80.9 ± 9.3 81.4 ± 8.3 0.5 ± 7.3 –1.55 (–3.37, 0.27) 0.09
Fasting glucose,3 mg/dL 136.4 ± 43 139 ± 50.8 2.8 ± 41.3 146.6 ± 54.9 146 ± 47.0 –0.5 ± 45.1 3.28 (–7.00, 13.57) 0.53
HbA1c,3 % 7.3 ± 1.2 7.4 ± 1.4 0.1 ± 0.9 7.8 ± 1.5 7.8 ± 1.4 0.0 ± 0.9 0.10 (–0.13, 0.32) 0.40
Insulin,3 µIU/mL 13.6 ± 6.7 14.1 ± 7.8 0.5 ± 6.6 15.2 ± 9.5 15.8 ± 12.6 0.5 ± 7.4 –0.06 (–1.73, 1.61) 0.95
HOMA-IR 4.6 ± 3.2 5.0 ± 3.6 0.4 ± 3.2 5.7 ± 4.6 5.7 ± 5.1 0.0 ± 3.8 0.33 (–0.51, 1.17) 0.44

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TG,3 mg/dL 143.0 ± 69.7 147 ± 70.5 4.3 ± 51.1 146.9 ± 62.9 147 ± 68.8 0.4 ± 62.2 3.87 (–9.64, 17.38) 0.57
TChol,3 mg/dL 161.5 ± 32.8 165 ± 34.9 3.3 ± 25.9 171.7 ± 35.5 170 ± 35.8 –1.9 ± 25.6 5.17 (–0.98, 11.31) 0.10
HDL cholesterol,3 mg/dL 38.4 ± 8.1 40.1 ± 7.9 1.7 ± 5.6 40.1 ± 7.9 40.2 ± 7.4 0.1 ± 4.6 1.58 (0.35, 2.80) 0.01
LDL cholesterol,3 mg/dL 94.6 ± 29 95.8 ± 29.9 0.9 ± 25.1 102.2 ± 31.1 99.2 ± 30.7 –3.0 ± 21.6 3.87 (–1.75, 9.49) 0.18
VLDL cholesterol,3 mg/dL 28.0 ± 12.6 28.4 ± 11.7 0.7 ± 9.5 29.4 ± 12.6 29.5 ± 13.7 0.1 ± 12.5 0.60 (–2.04, 3.25) 0.66
TChol:HDL cholesterol ratio 4.4 ± 1.2 4.2 ± 0.9 –0.2 ± 1.0 4.4 ± 1.1 4.3 ± 1.1 –0.1 ± 0.8 –0.09 (–0.31, 0.13) 0.41
1
Values are means ± SDs. DBP, diastolic blood pressure; HbA1c, glycated hemoglobin; SBP, systolic blood pressure; TChol, total cholesterol; TChol:HDL ratio, total cholesterol
to high-density lipoprotein cholesterol ratio; WC, waist circumference.
2
From linear models with robust variance estimation under an assumed independence working correlation.
3
HbA1c and fasting glucose are plasma analytes, whereas others (insulin, HDL cholesterol, LDL cholesterol, VLDL cholesterol, TG, TChol/HDL cholesterol ratio) are serum
analytes.

satiety acutely and reduce second meal consumption in adults
with impaired glucose tolerance. Future studies should evaluate
satiety as one potential mechanism underlying the observed lack
of weight gain among individuals consuming cashew nuts.
Substituting ∼15% of calories from pistachios (2–
3 ounces/d) for other sources of fat in the diet showed a
significant increase in HDL cholesterol and no change in total
cholesterol, LDL cholesterol, or TGs among adults with mild
hypercholesterolemia (41). In another parallel-arm, randomized
controlled trial, 30 g walnuts consumed as part of a modified
low-fat diet was associated with a significant increase in HDL
cholesterol among adults with T2DM (21). Trials testing the
effects of almonds and pistachios have also found a signifi-
cant increase in HDL cholesterol in mildly and moderately
hypercholesterolemic subjects (41, 42). In the present study,
it was observed that supplementation of 30 g cashew nuts/d
for 12 wk among adults with T2DM resulted in a significant
increase in HDL cholesterol (on average, 1.58 mg/dL) but no
significant changes in TGs, total cholesterol, or LDL choles-
terol. Considering that the seminal Framingham Heart Study
found that HDL cholesterol was the most important predictor
of heart disease among older men and women (43), and that
nearly three-fourths of Asian Indians have low HDL cholesterol
concentrations (4), our results have important clinical implica-
tions. Indeed, just a 1% increase in HDL cholesterol has been
associated with a 3% reduction in heart disease risk in previous
studies (44). The mechanism by which cashew nuts favorably
influence HDL cholesterol concentrations remains unclear.
Mensink et al. (45) reported that MUFA-rich diets increased
the level of apoA-I, and apoA-I has been demonstrated to
increase cholesterol efflux in THP-1-derived macrophages (46).
The increase in HDL cholesterol concentrations could also be
due to the fatty acid composition of the intervention diet with
subsequent decrease in carbohydrate intake as a percentage
of energy. Kris-Etherton et al. (47) reported that substituting
MUFAs for saturated fatty acids or carbohydrates tends to
increase HDL cholesterol concentrations. Cashew nuts are rich
in fat, predominantly MUFAs (∼60% of total fat) (22). This is
reflected in the significantly higher MUFA intake reported by
the intervention group compared to the control group in the
present study.
Our study showed a significantly greater decrease in SBP in
the intervention group compared to the control group. These
results are consistent with a large randomized controlled trial
conducted in the United States showing that partial replacement
of carbohydrate with MUFAs (10% calories from carbohydrate
replaced with 8% calories from MUFAs) reduces blood pressure
(48). A randomized controlled trial by Schutte et al. (49) found
that consuming unsalted cashew nuts (20% of energy) for 8 wk
improved the baroreflex sensitivity, a key mechanism for main-
taining healthy blood pressure, compared to walnut consump-
tion among participants with metabolic syndrome. Moreover,
in addition to fatty acids, several other nutritive components of
nuts may explain their benefits on metabolic and cardiovascular
outcomes. In particular, cashew nuts are high in the amino acid
arginine: 30 g cashew nuts provides 2.9 g arginine (50). Given
that arginine is a precursor for nitric oxide, an endogenous va-
sodilator (51), this may explain some of the observed beneficial
effect on SBP in this study. Indeed, a meta-analysis of 13 ran-
domized controlled trials testing the effects of oral l-arginine
supplements (ranging in dose from 6 to 63 g/d) on endothe-
lial function found significant overall improvements in flow-
mediated dilation (52), thus lending support to the hypothesized
protective cardiovascular effects of arginine in cashew nuts.
A recent systematic review (53) reported that studies with
MUFA intake >12% of energy conferred a significant reduction
in HbA1c. In our study, despite the 30 g cashew nut/d supple-
mentation, the total MUFA concentrations in the intervention
group (9% of total daily calories) was still far below the rec-
ommendations of 15–20% total daily calories. Whether posi-
tive effects on glycemia could be produced by consumption of
higher amounts of cashew nuts as part of a healthy diet needs
further investigation. A study by Lovejoy et al. (54) showed that
almond supplementation (57–113 g/d) in a high-fat diet (37%

Effect of cashew nuts on glycemic and lipid profile 67

calories from fat) resulted in greater reductions in HbA1c when
compared to similar almond supplementation in a low-fat diet
(25% calories from fat). Thus, the null effect on HbA1c in our
study could be due to the lower dose of cashew nuts (30 g/d) or
the lower total fat content of the diet (∼30%); further research
on the impact of nut supplementation on glycemia is warranted.
The present study has several strengths. First, the partici-
pants’ overall compliance to the study was good, with a dropout
rate of only ∼10%. Second, dietary compliance was measured
both by nutrient biomarker (plasma oleic acid) and self-reported
dietary intake of oleic acid, MUFAs, and nuts. These were sig-
nificantly higher in the intervention group compared to the con-
trol group, suggesting good adherence. This could explain the
positive changes in HDL cholesterol in the intervention group.
Well-trained dietitians collected the data through face-to-face
interviews. However, the study also has a few limitations. Al-
though we advised the participants to adhere to the study pro-
tocol and not to make major lifestyle and dietary changes, in
a community-based trial such as this, family and environmen-
tal influences such as festivals and marriage feasts might have
had some impact on the results. These effects would be likely
to occur in both groups, biasing results towards the null. The
24-h dietary recall collected during the study to assess partici-
pants’ adherence could have suffered from recall bias or might
not have reflected typical intake. Because Indian diets are usually
low in oleic acid (8), we used plasma concentrations of oleic acid
as a proxy of its intake in our study. However, we acknowledge
that plasma levels of oleic acid depend not only on the intake but
also on the endogenous synthesis; therefore, this cannot be con-
sidered a good marker of consumption. The levels of fatty acids
in adipocytes or erythrocytes are considered more accurate and
reliable markers of intake in the medium and long term than
plasma levels. Despite this, the plasma concentrations of fatty
acids have been used in large studies as a measure of compliance
(55). The lack of a significant correlation between plasma levels
of oleic acid and changes in HDL cholesterol is not surprising
because, as pointed out above, plasma concentrations of oleic
acid reflect individual differences in endogenous synthesis and
metabolism, and are only weakly correlated with dietary intake
of this fatty acid (56). Thus, other nutrient biomarkers should
be explored in the future as markers of individual compliance
to nut supplement trials; on a group basis, changes in plasma
oleic acid can be a useful qualitative indicator of compliance.
One might argue whether the results obtained would have
been different if higher quantities of nuts had been used. For this
reason, it will be interesting in the future to analyze if the effects
of nut consumption on glycemia, lipids, and other risk factors
of CVD are dose dependent. Finally, due to budget constraints,
we were not able to assess apo proteins such as apoA-I. Future
studies should expand the panel of biomarkers assessed in order
to further elucidate potential biological mechanisms underlying
observed associations.
In conclusion, this study reports that in Asian Indians with
T2DM, regular consumption of 30 g cashew nuts decreased SBP
and increased HDL cholesterol concentrations with no undesir-
able effects on body weight, glycemia, or other lipid variables.
Supplementation of Indian diets with cashew nuts could help to
improve the Asian Indian phenotype of dyslipidemia with low
HDL concentrations, which is an important CVD risk factor
contributing to premature CVD in this population.
Acknowledgements
We thank Ruchi Vaidya for her help in standardizing the pro-
tocol for the plasma markers and Kalpana Natarajan for her
68 Mohan et al.
field support and bibliographical assistance. We also acknowl-
edge the help and support of clinical dieticians Thangamani and
Jaishree at Dr. Mohan’s Diabetes Specialities Centre, as well as
information technology team member Ezhilarasi for developing
unique software for this study, and the clinical laboratory team
for their support in biochemical assessments. The authors’ re-
sponsibilities were as follows—VM, RMA, and VS: conceived
the study; KK, JSS, WCW, and DS: reviewed the protocol of the
study; RG, SD, and VK: executed the trial; RGJ, KKB, SS, MJ,
MRB, and VG: assessed plasma biomarkers; LMJ, RG, NL, and
PV: performed the statistical analysis; DS: assisted with the sta-
tistical analysis plan and interpretation; VM, WCW, KK, RMA,
RU, LMJ, and VS: further assisted in interpretation; RG: initi-
ated the manuscript and LMJ further assisted and revised; and
a all authors: critically reviewed the manuscript and approved
the final version.
Downloaded from https://academic.oup.com/jn/article-abstract/148/1/63/4823695 by guest on 20 March 2019
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Effect of cashew nuts on glycemic and lipid profile 69